ArticleFree radical biology & medicine
17β-Estradiol prevents cell death and mitochondrial dysfunction by an estrogen receptor-dependent mechanism in astrocytes after oxygen-glucose deprivation/reperfusion.
Article in Free radical biology & medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 81 citations in OpenAlex.
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- Sex differences in the inflammatory response to stroke.Seminars in immunopathology · 2023Review
- Non-genomic Effect of Estradiol on the Neurovascular Unit and Possible Involvement in the Cerebral Vascular Accident.Molecular neurobiology · 2023Review
- Early post-stroke cognitive impairment and in-hospital predicting factors among stroke survivors in Ethiopia.Frontiers in neurology · 2023Article
- Immune regulation based on sex differences in ischemic stroke pathology.Frontiers in immunology · 2023Review
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- Estrogen alleviates hepatocyte necroptosis depending on GPER in hepatic ischemia reperfusion injury.Journal of physiology and biochemistry · 2022Article
- Sex-Associated Differences in Neurovascular Dysfunction During Ischemic Stroke.Frontiers in molecular neuroscience · 2022Review
- Sex differences in post-stroke cognitive decline: A population-based longitudinal study of nationally representative data.PloS one · 2022Article
- Sex differences in recovery of motor function in a rhesus monkey model of cortical injury.Biology of sex differences · 2021Article
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- Changes in Inflammatory Response, Redox Status and NaNeurotoxicity research · 2020Article
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- Dual Roles of Astrocyte-Derived Factors in Regulation of Blood-Brain Barrier Function after Brain Damage.International journal of molecular sciences · 2019Review
- Insulin-like Growth Factor (IGF)-1 treatment stabilizes the microvascular cytoskeleton under ischemic conditions.Experimental neurology · 2019Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
17β-Estradiol (E2) has been shown to protect against ischemic brain injury, yet its targets and the mechanisms are unclear. E2 may exert multiple regulatory actions on astrocytes that may greatly contribute to its ability to protect the brain. Mitochondria are recognized as playing central roles in the development of injury during ischemia. Increasing evidence indicates that mitochondrial mechanisms are critically involved in E2-mediated protection. In this study, the effects of E2 and the role of mitochondria were evaluated in primary cultures of astrocytes subjected to an ischemia-like condition of oxygen-glucose deprivation (OGD)/reperfusion. We showed that E2 treatment significantly protects against OGD/reperfusion-induced cell death as determined by cell viability, apoptosis, and lactate dehydrogenase leakage. The protective effects of E2 on astrocytic survival were blocked by an estrogen receptor (ER) antagonist (ICI-182,780) and were mimicked by an ER agonist selective for ERα (PPT), but not by an ER agonist selective for ERβ (DPN). OGD/reperfusion provoked mitochondrial dysfunction as manifested by an increase in cellular reactive oxygen species production, loss of mitochondrial membrane potential, and depletion of ATP. E2 pretreatment significantly inhibited OGD/reperfusion-induced mitochondrial dysfunction, and this effect was also blocked by ICI-182,780. Therefore, we conclude that E2 provides direct protection to astrocytes from ischemic injury by an ER-dependent mechanism, highlighting an important role for ERα. Estrogen protects against mitochondrial dysfunction at the early phase of ischemic injury. However, overall implications for protection against brain ischemia and its complex sequelae await further exploration.
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Registered trials
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